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Article

Haploinsufficiency of Gtf2i, a gene deleted in Williams Syndrome, leads to increases in social interactions.

Autism research : official journal of the International Society for Autism Research - 1 Feb 2011

Sakurai Takeshi, Dorr Nathan P, Takahashi Nagahide, McInnes L Alison, Elder Gregory A, Buxbaum Joseph D

Abstract excerpt

Identifying genes involved in social behavior is important for autism research. Williams-Beuren syndrome (WBS) is a developmental syndrome with unique neurocognitive features, including low IQ, deficits in visuospatial and visual-motor abilities, hypersensitivity to sounds, hypersociability, and increased general anxiety. The syndrome is caused by a recurrent hemizygous deletion of the 7q11.23 region, containing...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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PMID: 21328569
DOI: 10.1002/aur.169

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Haploinsufficiency of Gtf2i, a gene deleted in Williams Syndrome, leads to increases in social interactions.PMID 21328569Read ↗

Consistent hypersocial behavior in mice carrying a deletion of Gtf2i but no evidence of hyposocial behavior with Gtf2i duplication: Implications for Williams-Beuren syndrome and autism spectrum disorder.Semantic proximity Read ↗

Cognitive-behavioral phenotypes of Williams syndrome are associated with genetic variation in the GTF2I gene, in a healthy population.Semantic proximity Read ↗

<i>Gtf2i</i> and <i>Gtf2ird1</i> mutation are not sufficient to reproduce mouse phenotypes caused by the Williams Syndrome critical regionSemantic proximity Read ↗

Anxious, hypoactive phenotype combined with motor deficits in Gtf2ird1 null mouse model relevant to Williams syndrome.Semantic proximity Read ↗

Duplication of GTF2I results in separation anxiety in mice and humans.Semantic proximity Read ↗

The contribution of GTF2I haploinsufficiency to Williams syndrome.Semantic proximity Read ↗

Global analysis of gene expression in the developing brain of Gtf2ird1 knockout mice.Semantic proximity Read ↗

Intracisternal Gtf2i Gene Therapy Ameliorates Deficits in Cognition and Synaptic Plasticity of a Mouse Model of Williams-Beuren Syndrome.Semantic proximity Read ↗

Induced chromosome deletions cause hypersociability and other features of Williams-Beuren syndrome in mice.Semantic proximity Read ↗

Contrasting behavioral and physiological effects of <i>Gtf2i</i> duplication and deletion in mouse models of the 7q11.23 Duplication and Williams-Beuren SyndromesSemantic proximity Read ↗

Extensive characterization of a Williams Syndrome murine model shows <i>Gtf2ird1</i> -mediated rescue of select sensorimotor tasks, but no effect on enhanced social behaviorSemantic proximity Read ↗

Mutation of Gtf2ird1 from the Williams-Beuren syndrome critical region results in facial dysplasia, motor dysfunction, and altered vocalisations.Semantic proximity Read ↗

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